Journal article
Differential responses to Ig and class II-mediated signals in splenic B cell subsets from normal and autoimmune mice
International immunology, Vol.6(7), pp.1049-1059
07/1994
DOI: 10.1093/intimm/6.7.1049
PMID: 7947456
Abstract
B cells of mouse and human can be divided into distinct subpopulations, differing in distribution and phenotype. It is not known, however, whether B cell subsets respond similarly to signals mediated by cognate interactions with T cells, such as ligation of the B cell class II MHC molecule. Mouse splenic B cells proliferate in response to a combination of non-mitogenic anti-mu mAb, IL-4 and class II MHC-specific mAbs. In order to assess the response of B cell subpopulations to these signals, B cells were separated on the basis of CD23 expression. Previous studies have shown that CD23 expression is useful in distinguishing marginal zone from follicular B cells and peritoneal B1 from B2 B cells. B cells of both subsets responded to the combination of signals, but CD23- B cells showed a higher response. Splenic B cells were also purified from several strains of autoimmune mice, of interest because their disease features expansion of CD23- B cells and autoantibody production. While normal B cells showed no response to non-mitogenic anti-mu mAb alone, B cells from autoimmune mice showed a marked decrease in proliferation. Addition of IL-4 plus class II-specific mAbs restored increased proliferation. Again, responses were higher in CD23- than in CD23+ B cells. These findings suggest that CD23- B cells are especially responsive to signals delivered through class II and the IL-4 receptor. These signals may allow preferential rescue of CD23-B cells from antigen-mediated tolerance and result in their hyperexpansion in response to autoreactive T cells.
Details
- Title: Subtitle
- Differential responses to Ig and class II-mediated signals in splenic B cell subsets from normal and autoimmune mice
- Creators
- Gail A Bishop - Department of Microbiology, University of Iowa, Iowa City 52242Luis M RamirezThomas J Waldschmidt
- Resource Type
- Journal article
- Publication Details
- International immunology, Vol.6(7), pp.1049-1059
- Publisher
- England
- DOI
- 10.1093/intimm/6.7.1049
- PMID
- 7947456
- ISSN
- 0953-8178
- eISSN
- 1460-2377
- Grant note
- AI28847 / NIAID NIH HHS AI31265 / NIAID NIH HHS
- Language
- English
- Date published
- 07/1994
- Academic Unit
- Microbiology and Immunology; President; Pathology
- Record Identifier
- 9984002375702771
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